Brain functions typically involve precise circuits with nodes interconnected over long distances. Thus a brain lesion can interrupt one node in a circuit, leaving the other nodes intact but rendering the overall circuit inoperable. Lesions in the brain typically occur as a result of events such as strokes and traumatic brain injury.
One specific form of brain damage is the deficit of neglect. Neglect is commonly a result of damage to the posterior parietal cortex (PPC). Patients ignore or are not aware of the contralateral space, particularly left space for right parietal damage. A popular competition theory has been proposed for neglect in which the two cerebral hemispheres each process information in the contralateral space and they compete with one another for the distribution of attention and awareness. If one hemisphere is damaged then the other has an advantage and the patient is biased toward the healthy visual field and unable to process information in the unhealthy part of space.
Another deficit is optic ataxia, which is caused by lesions in the human PPC. Optic ataxia (OA) impairs reaches but not saccades (eye movements) to visual objects. It has been suggested that there are separate visuomotor pathways for the two effectors of limbs (reaches) and eyes (saccades). In monkeys, one potentially crucial area for reach control is the parietal reach region (PRR), in which neurons respond preferentially during reach planning as compared to saccade planning. Direct causal evidence linking the monkey PRR to the deficits observed in OA has recently been shown in inactivation studies (Hwang, et al., “Inactivation of the Parietal Reach Region Causes Optic Ataxia, Impairing Reaches but Not Saccades” Neuron, Vol. 76, pp. 1021-29, Dec. 6, 2012). Lesions to Brodmann's area 5 also produce OA.
There is therefore a need for a method of brain repair that utilizes healthy nodes to compensate for damaged nodes. There is a further need for a system based on studies of brain circuits to determine likely nodes for stimulation to repair damage from brain lesions resulting in deficits.